Based on the findings of this study, we therefore propose that HDAC7 appears to be a potential therapeutic target in pre-B-ALL, and this small molecular compound CC1007 could inhibit tumor growth, induce cycle arrest and differentiation of BCR-ABL1− pre-B-ALL cells, and to prolong the survival of BCR-ABL1− pre-B-ALL-bearing mice, partially by inhibiting HDAC7 expression and HDAC7:MEF2C interaction, indicating that CC1007 may be a promising agent for the treatment of BCR-ABL1− pre-B-ALL. Here, BCR is linked to acute lymphoblastic leukemia.